Analgesic doses of morphine and viminol R2 increase striatal dopamine turnover rate but this increase does not appear related to either an increase in the firing rate of dopaminergic neurons or to the stimulation of postsynaptic dopaminergic receptors. However, morphine blocks the activation of striatal TH induced by neuroleptic drugs. Morphine, viminol R2, azidomorphine increase cGMP in striatum and accumbens but not in cerebellum. The changes of cGMP in striatum and accumbens are blocked by naloxone. Thus activation of the cGMP system can represent the specific synaptic response following an interaction of the opiate receptor with its antagonist. The location of the opiate receptors and the relation of opiate receptor function with the DA neurons in substantia nigra and striatum is now under investigation. BIBLIOGRAPHIC REFERENCES: Racagni, G., Zsilla, G., Guidotti, A. and Costa, E.: Accumulation of cGMP in striatum of rats injected with narcotic analgesics: Antagonism by naltrexone. J. Pharm. Pharmacol. 28: 258-260, 1976. Biggio, G., Guidotti, A. and Costa, E.: On the mechanism of the decrease in cerebellar cGMP content elicited by opiate receptor agonists. Naunyn Schmied. Arch. Pharmacol. 296: 117-121, 1977.